The organometals have numerous applications in industrial and occupational settings. The neurotoxicity of these agents, particularly organoleads and tins, is well known. However, their precise sites and mechanisms of action are poorly understood. The purpose of these studies is to characterize the neurophysiological effects of relevant organometals in an attempt to determine the site of action and aid in determining the mechanism of action of selected organometals. We have found that triethyl lead (TEL), but not trimethyl lead, triethyl tin or trimethyl tin markedly increases the sensitivity to pentylenetetrazol induced seizures. This increase in sensitivity is most pronounced in animals receiving multiple pentylenetetrazol injections. There is little, if any, change in sensitivity to a single dose of pentylenetetrazol. Thus, the most striking effect of TEL appears to be an acceleration of the pentylenetetrazol kindling process. This effect of TEL can be attenuated by anticholinergic agents (atropine and scopolamine). Assessment of the neurophysiological and neurochemical bases for pentylenetetrazol-induced kindling and the mechanisms whereby TEL exacerbates it should further our knowledge of excitatory phenomena of the nervous system and how these can be altered by neurotoxic substances.